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Therapeutic potential of autophagy-enhancing agents in Parkinson’s disease

Overview of attention for article published in Molecular Neurodegeneration, January 2017
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (83rd percentile)
  • Average Attention Score compared to outputs of the same age and source

Mentioned by

news
1 news outlet
twitter
1 tweeter

Readers on

mendeley
167 Mendeley
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Title
Therapeutic potential of autophagy-enhancing agents in Parkinson’s disease
Published in
Molecular Neurodegeneration, January 2017
DOI 10.1186/s13024-017-0154-3
Pubmed ID
Authors

Tim E. Moors, Jeroen J. M. Hoozemans, Angela Ingrassia, Tommaso Beccari, Lucilla Parnetti, Marie-Christine Chartier-Harlin, Wilma D. J. van de Berg

Abstract

Converging evidence from genetic, pathological and experimental studies have increasingly suggested an important role for autophagy impairment in Parkinson's Disease (PD). Genetic studies have identified mutations in genes encoding for components of the autophagy-lysosomal pathway (ALP), including glucosidase beta acid 1 (GBA1), that are associated with increased risk for developing PD. Observations in PD brain tissue suggest an aberrant regulation of autophagy associated with the aggregation of α-synuclein (α-syn). As autophagy is one of the main systems involved in the proteolytic degradation of α-syn, pharmacological enhancement of autophagy may be an attractive strategy to combat α-syn aggregation in PD. Here, we review the potential of autophagy enhancement as disease-modifying therapy in PD based on preclinical evidence. In particular, we provide an overview of the molecular regulation of autophagy and targets for pharmacological modulation within the ALP. In experimental models, beneficial effects on multiple pathological processes involved in PD, including α-syn aggregation, cell death, oxidative stress and mitochondrial dysfunction, have been demonstrated using the autophagy enhancers rapamycin and lithium. However, selectivity of these agents is limited, while upstream ALP signaling proteins are involved in many other pathways than autophagy. Broad stimulation of autophagy may therefore cause a wide spectrum of dose-dependent side-effects, suggesting that its clinical applicability is limited. However, recently developed agents selectively targeting core ALP components, including Transcription Factor EB (TFEB), lysosomes, GCase as well as chaperone-mediated autophagy regulators, exert more specific effects on molecular pathogenetic processes causing PD. To conclude, the targeted manipulation of downstream ALP components, rather than broad autophagy stimulation, may be an attractive strategy for the development of novel pharmacological therapies in PD. Further characterization of dysfunctional autophagy in different stages and molecular subtypes of PD in combination with the clinical translation of downstream autophagy regulation offers exciting new avenues for future drug development.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 167 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 <1%
Unknown 166 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 32 19%
Researcher 28 17%
Student > Master 24 14%
Student > Bachelor 21 13%
Student > Postgraduate 11 7%
Other 26 16%
Unknown 25 15%
Readers by discipline Count As %
Neuroscience 37 22%
Biochemistry, Genetics and Molecular Biology 34 20%
Agricultural and Biological Sciences 23 14%
Medicine and Dentistry 19 11%
Pharmacology, Toxicology and Pharmaceutical Science 7 4%
Other 15 9%
Unknown 32 19%

Attention Score in Context

This research output has an Altmetric Attention Score of 10. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 03 February 2017.
All research outputs
#1,033,324
of 9,003,777 outputs
Outputs from Molecular Neurodegeneration
#138
of 441 outputs
Outputs of similar age
#51,272
of 309,651 outputs
Outputs of similar age from Molecular Neurodegeneration
#11
of 23 outputs
Altmetric has tracked 9,003,777 research outputs across all sources so far. Compared to these this one has done well and is in the 88th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 441 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.2. This one has gotten more attention than average, scoring higher than 64% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 309,651 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 83% of its contemporaries.
We're also able to compare this research output to 23 others from the same source and published within six weeks on either side of this one. This one is in the 39th percentile – i.e., 39% of its contemporaries scored the same or lower than it.